ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Neutrophils promote alveolar epithelial regeneration by enhancing type II pneumocyte proliferation in a model of acid-induced acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- The role of myeloid immune cells in lung epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- A precision approach to translational research in acute lung injury.American journal of respiratory and critical care medicine · 2026Article
- Culture conditions differentially regulate the inflammatory niche and cellular phenotype of tracheobronchial basal stem cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- The Importance of Lung Innate Immunity During Health and Disease.Pathogens (Basel, Switzerland) · 2025Review
- Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation.Frontiers in immunology · 2025Review
- Molecular signatures of alveolar type II cell differentiation in acute respiratory distress syndrome.Frontiers in medicine · 2025Article
- Neutrophil dynamics in pulmonary fibrosis: pathophysiological and therapeutic perspectives.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Culture Conditions Differentially Regulate the Inflammatory Niche and Cellular Phenotype of Tracheo-Bronchial Basal Stem Cells.bioRxiv : the preprint server for biology · 2024Article
- Beyond host defense and tissue injury: the emerging role of neutrophils in tissue repair.American journal of physiology. Cell physiology · 2024Review
- Gasdermin E dictates inflammatory responses by controlling the mode of neutrophil death.Nature communications · 2024Article
- The emerging role for neutrophil mitochondrial metabolism in lung inflammation.Immunometabolism (Cobham, Surrey) · 2024Review
- Neutrophil diversity and plasticity: Implications for organ transplantation.Cellular & molecular immunology · 2023Review
- Mesenchymal stem cells shift the pro-inflammatory phenotype of neutrophils to ameliorate acute lung injury.Stem cell research & therapy · 2023Article
- Single-cell RNA sequencing reveals the dynamics of hepatic non-parenchymal cells in autoprotection against acetaminophen-induced hepatotoxicity.Journal of pharmaceutical analysis · 2023Article
- Immunomodulation for Tissue Repair and Regeneration.Tissue engineering and regenerative medicine · 2023Review
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
- Immunological evaluation of patients with 2019 novel coronavirus pneumonia: CD4+ and CD16+ cells may predict severity and prognosis.PloS one · 2022Article
- Connecting the dots: Neutrophils at the interface of tissue regeneration and cancer.Seminars in immunology · 2021Review
- Small extracellular vesicle-mediated bidirectional crosstalk between neutrophils and tumor cells.Cytokine & growth factor reviews · 2021Review
- Understanding the role of neutrophils in acute respiratory distress syndrome.Biomedical journal · 2021Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Alveolar epithelial regeneration is essential for resolution of the acute respiratory distress syndrome (ARDS). Although neutrophils have traditionally been considered mediators of epithelial damage, recent studies suggest they promote type II pneumocyte (AT2) proliferation, which is essential for regenerating alveolar epithelium. These studies did not, however, evaluate this relationship in an in vivo model of alveolar epithelial repair following injury. To determine whether neutrophils influence alveolar epithelial repair in vivo, we developed a unilateral acid injury model that creates a severe yet survivable injury with features similar to ARDS. Mice that received injections of the neutrophil-depleting Ly6G antibody had impaired AT2 proliferation 24 and 72 h after acid instillation, which was associated with decreased reepithelialization and increased alveolar protein concentration 72 h after injury. As neutrophil depletion itself may alter the cytokine response, we questioned the contribution of neutrophils to alveolar epithelial repair in neutropenic granulocyte-colony stimulating factor (G-CSF)-/- mice. We found that the loss of G-CSF recapitulated the neutrophil response of Ly6G-treated mice and was associated with defective alveolar epithelial repair, similar to neutrophil-depleted mice, and was reversed by administration of exogenous G-CSF. To approach the mechanisms, we employed an unbiased protein analysis of bronchoalveolar lavage fluid from neutrophil-depleted and neutrophil-replete mice 12 h after inducing lung injury. Pathway analysis identified significant differences in multiple signaling pathways that may explain the differences in epithelial repair. These data emphasize an important link between the innate immune response and tissue repair in which neutrophils promote alveolar epithelial regeneration.
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Registered trials
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